Do we actually know how much we DON’T KNOW about the COVID-19?

While Governments, doctors, and even specialists are desperately trying to better understand this pandemic, there are many posts and articles all over the internet trying to make sense of the Coronavirus reality. In situations like that, sometimes, out-of-the-box thinking can be the one thing that makes a real difference.

My business partner on Start-A-Biz-Now (, Dan Nichols, emailed me an article with a personal note saying “Interesting if true. Worth the read.“. Dan is a good friend and a very intelligent person. So, when I got such a message from him, I wasted no time and went after to read it.

The article in question was titled “COVID-19 had us all fooled, but now we might have finally found its secret.“. A very “suggestive” title that I could easily have passed if it wasn’t for Dan’s recommendation. Why? Because I stumble upon crazy theories about everything all over the internet all the time. It always amazes me how some people find time to write oddly convincing posts and articles that, in most cases, are nothing more than a bunch of mumbo-jumbo, pure crap.

However, it doesn’t seem to be the case of the article referenced by Dan. In fact, when I finished reading it, I found myself scratching my head and extremely curious about what it proposes, which made me switch to research mode.

To make it short, it was fairly easy to find others like me who read the same article and tried to validate (or discredit) what was proposed in it. My objective here is to bring forward a combination of the original article and some important findings that makes it a valid discussion.

Be advised, however, that no one has confirmed – neither discarded – what is proposed in the article. Read it with caution. Even if surrounded by what apparently may be coherent statements, the text may be entirely fictional or incorrect. 

The article below has the entire original post excluding only those few paragraphs in which the author promoted his “political agenda”, that is irrelevant for the main proposed discussion. The original text, if you rather read it, can be found here.

COVID-19 had us all fooled, but now we might have finally found its secret

By libertymavenstock

Published on April 5 (Original post is now offline)

In the last 3–5 days, a mountain of anecdotal evidence has come out of NYC, Italy, Spain, etc. about COVID-19 and the characteristics of patients who get seriously ill. It’s not only piling up but now leading to a general field-level consensus backed up by a few previously little-known studies that we’ve had it all wrong the whole time. Well, a few had some things eerily correct (cough Trump cough), especially with Hydroxychloroquine with Azithromycin, but we’ll get to that in a minute.

There is no ‘pneumonia’ nor ARDS. At least not the ARDS with established treatment protocols and procedures we’re familiar with. Ventilators are not only the wrong solution, but high-pressure intubation can actually wind up causing more damage than without, not to mention complications from tracheal scarring and ulcers given the duration of intubation often required… They may still have a use in the immediate future for patients too far to bring back with this newfound knowledge, but moving forward a new treatment protocol needs to be established so we stop treating patients for the wrong disease.

The past 48 hours or so have seen a huge revelation: COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing o2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of ARDS or pneumonia. All the damage to the lungs you see in CT scans are from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs. Patients returning for re-hospitalization days or weeks after recovery suffering from apparent delayed post-hypoxic leukoencephalopathy strengthen the notion COVID-19 patients are suffering from hypoxia despite no signs of respiratory ‘tire out’ or fatigue.

Here’s the breakdown of the whole process, including some ELI5-level cliff notes. Much has been simplified just to keep it digestible and layman-friendly.

Your red blood cells carry oxygen from your lungs to all your organs and the rest of your body. Red blood cells can do this thanks to hemoglobin, which is a protein consisting of four “hemes”. Hemes have a special kind of iron ion, which is normally quite toxic in its free form, locked away in its center with a porphyrin acting as it’s ‘container’. In this way, the iron ion can be ‘caged’ and carried around safely by the hemoglobin, but used to bind to oxygen when it gets to your lungs.

When the red blood cell gets to the alveoli or the little sacs in your lungs where all the gas exchange happens, that special little iron ion can flip between FE2+ and FE3+ states with electron exchange and bond to some oxygen, then it goes off on its little merry way to deliver o2 elsewhere.

Here’s where COVID-19 comes in. Its glycoproteins bond to the heme, and in doing so that special and toxic oxidative iron ion is “disassociated” (released). It’s basically let out of the cage and now freely roaming around on its own. This is bad for two reasons:

  1. Without the iron ion, hemoglobin can no longer bind to oxygen. Once all the hemoglobin is impaired, the red blood cell is essentially turned into a Freightliner truck cab with no trailer and no ability to store its cargo.. it is useless and just running around with COVID-19 virus attached to its porphyrin. All these useless trucks running around not delivering oxygen is what starts to lead to desaturation, or watching the patient’s spo2 levels drop. It is INCORRECT to assume traditional ARDS and in doing so, you’re treating the WRONG DISEASE. Think of it a lot like carbon monoxide poisoning, in which CO is bound to the hemoglobin, making it unable to carry oxygen. In those cases, ventilators aren’t treating the root cause; the patient’s lungs aren’t ‘tiring out’, they’re pumping just fine. The red blood cells just can’t carry o2, end of the story. Only in this case, unlike CO poisoning in which eventually the CO can break off, the affected hemoglobin is permanently stripped of its ability to carry o2 because it has lost its iron ion. The body compensates for this lack of o2 carrying capacity and deliveries by having your kidneys release hormones like erythropoietin, which tell your bone marrow factories to ramp up production on new red blood cells with freshly made and fully functioning hemoglobin. This is the reason you find elevated hemoglobin and decreased blood oxygen saturation as one of the 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.
  2. That little iron ion, along with millions of its friends released from other hemes, is now floating through your blood freely. As I mentioned before, this type of iron ion is highly reactive and causes oxidative damage. It turns out that this happens to a limited extent naturally in our bodies and we have cleanup & defense mechanisms to keep the balance. The lungs, in particular, have 3 primary defenses to maintain “iron homeostasis”, 2 of which are in the alveoli, those little sacs in your lungs we talked about earlier. The first of the two is little macrophages that roam around and scavenge up any free radicals like this oxidative iron. The second is a lining on the walls (called the epithelial surface) which has a thin layer of fluid packed with high levels of antioxidant molecules.. things like abscorbic acid (AKA Vitamin C) among others. Well, this is usually good enough for naturally occurring rogue iron ions but with COVID-19 running rampant your body is now basically like a progressive state letting out all the prisoners out of the prisons… it’s just too much iron and it begins to overwhelm your lungs’ countermeasures, and thus begins the process of pulmonary oxidative stress. This leads to damage and inflammation, which leads to all that nasty stuff and damage you see in CT scans of COVID-19 patient lungs. Ever noticed how it’s always bilateral? (both lungs at the same time) Pneumonia rarely ever does that, but COVID-19 does… EVERY SINGLE TIME.

Once your body is now running out of control, with all your oxygen trucks running around without any freight, and tons of this toxic form of iron floating around in your bloodstream, other defenses kick in. While your lungs are busy with all this oxidative stress they can’t handle, and your organs are being starved of o2 without their constant stream of deliveries from red blood cell’s hemoglobin, and your liver is attempting to do its best to remove the iron and store it in its ‘iron vault’. Only its getting overwhelmed too. It’s starved for oxygen and fighting a losing battle from all your hemoglobin letting its iron free, and starts crying out “help, I’m taking damage!” by releasing an enzyme called alanine aminotransferase (ALT). BOOM, there is your second of 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

Eventually, if the patient’s immune system doesn’t fight off the virus in time before their blood oxygen saturation drops too low, ventilator or no ventilator, organs start shutting down. No fuel, no work. The only way to even try to keep them going is max oxygen, even a hyperbaric chamber if one is available on 100% oxygen at multiple atmospheres of pressure, just to give what’s left of their functioning hemoglobin a chance to carry enough o2 to the organs and keep them alive. Yeah we don’t have nearly enough of those chambers, so some fresh red blood cells with normal hemoglobin in the form of a transfusion will have to do.

The core point being, treating patients with the iron ions stripped from their hemoglobin (rendering it abnormally nonfunctional) with ventilator intubation is futile, unless you’re just hoping the patient’s immune system will work its magic in time. The root of the illness needs to be addressed.

Best case scenario? Treatment regimen early, before symptoms progress too far. Hydroxychloroquine (more on that in a minute, I promise) with Azithromycin has shown fantastic, albeit critics keep mentioning ‘anecdotal’ to describe the mountain, promise and I’ll explain why it does so well next. But forget straight-up plasma with antibodies, that might work early but if the patient is too far gone they’ll need more. They’ll need all the blood: antibodies and red blood cells. No help in sending over a detachment of ammunition to a soldier already unconscious and bleeding out on the battlefield, you need to send that ammo along with some hemoglobin-stimulant-magic so that he can wake up and fire those shots at the enemy.

The story with Hydroxychloroquine

How does chloroquine work? Same way as it does for malaria. You see, malaria is this little parasite that enters the red blood cells and starts eating hemoglobin as its food source. The reason chloroquine works for malaria is the same reason it works for COVID-19 — while not fully understood, it is suspected to bind to DNA and interfere with the ability to work magic on hemoglobin. The same mechanism that stops malaria from getting its hands on hemoglobin and gobbling it up seems to do the same to COVID-19 (essentially little snippets of DNA in an envelope) from binding to it. On top of that, Hydroxychloroquine (an advanced descendant of regular old chloroquine) lowers the pH which can interfere with the replication of the virus. Again, while the full details are not known, the entire premise of this potentially ‘game-changing’ treatment is to prevent hemoglobin from being interfered with, whether due to malaria or COVID-19.

No longer can the media and armchair pseudo-physicians sit in their little ivory towers, proclaiming “DUR so stoopid, malaria is bacteria, COVID-19 is a virus, anti-bacteria drug no work on the virus!”. They never got the memo that a drug doesn’t need to directly act on the pathogen to be effective. Sometimes it’s enough just to stop it from doing what it does to hemoglobin, regardless of the means it uses to do so.

Anyway, enough of the rant. What’s the end result here? First, the ventilator emergency needs to be re-examined. If you’re putting a patient on a ventilator because they’re going into a coma and need mechanical breathing to stay alive, okay we get it. Give ’em time for their immune systems to pull through. But if they’re conscious, alert, compliant — keep them on O2. Max it if you have to. If you HAVE to inevitably ventilate, do it at low pressure but max O2. Don’t tear up their lungs with max PEEP, you’re doing more harm to the patient because you’re treating the wrong disease.

Ideally, some form of treatment needs to happen to:

  1. Inhibit viral growth and replication. Here plays CHQ+ZPAK+ZINC or other retroviral therapies being studies. Less virus, less hemoglobin losing its iron, less severity and damage.
  2. Therapies used for anyone with abnormal hemoglobin or malfunctioning red blood cells. Blood transfusions. Whatever, I don’t know the full breadth and scope because I’m not a physician. But think along those lines, and treat the real disease. If you’re thinking about giving them plasma with antibodies, maybe if they’re already in bad shape think again and give them BLOOD with antibodies, or at least blood followed by plasma with antibodies.
  3. Now that we know more about how this virus works and affects our bodies, a whole range of options should open up.

My first question after reading the above article was “Who is this libertymavenstock?“. It took me virtually no time to find Kate’s post on a blog called “Small Dead Animals” where she brought up the same question and, for my delight, an answer. 

Based on Kate’s discovery, “libertymavenstock” is a Youtuber that deals with cryptocurrencies who’s real name is Andrew Gaiziunas. In a conversation with Kate, Andrew explains he wrote the article with the help of his father, a retired Illinois doctor of the same name. 

In his message, Andrew says the following:

Me and my dad (retired M.D.) were intrigued by the possibilities behind a particular piece of research coming across my desk yesterday morning (link to the referred research).

Being all stuck at home under quarantine, we wanted to learn more. My dad provided the medical knowledge, I provided the tech & sleuthing skills, and we came up with this core hypothesis. As we pulled together a series of anecdotal data, some pre-prints, and even some peer-reviewed papers, a clearer picture of the hypothesis formed. We found missing pieces precisely where we thought we would. And yes, we became convinced this is not only plausible but quite likely (or a similar mechanic) to be the case.

I threw it up on Medium just to save a copy and see if anyone would have feedback. We got plenty — much over both of our heads, some out-of-left-field fantastic ideas. For example, if this turns out to be the case, and hyperbaric oxygen therapy might save lives (we have far fewer hyperbaric chambers in the US than ICU beds), a mountain climber suggested portable hyperbaric bags which are pretty cheap (in comparison) and can fit through hospital doors could do the trick.

This was precisely the type of interaction we were looking for.

The article has since been taken down by Medium, but it seems it garnered sufficient interest in the 12 hours it was up as to be handed off to much more qualified and experienced hands. We’re hopeful some of this can be found to be useful; it may or may not, but NOT sharing it would have weighed heavier on our minds if we found out later this theory, or something similar to it, could have helped save lives and yet we did nothing about it.

Cheers and best of luck, everyone stay safe and thanks.


The reason I am referencing Kate’s post is that she brought forward a fair amount of links and good quality information about the proposed discussion. You may check out kate’s blog and post by clicking here.

Among many facts about the proposed discussion, Kate was also the person who found the video below, which is from a real doctor who treats COVID-19 patients in New York City. In the video, Dr. Cameron Kyle-Sidell tries to promote the following urgent message:

Patients need OXYGEN, NOT PRESSURE!!! The ventilators may be causing lung damage because of PRESSURE. Needs to be immediately investigated. 100,000 – 250,000 Americans at risk of lung injury.

Here you can watch Dr. Cameron’s entire video in which he explains his observations using his own words:

Among other dissertations about this subject, Dr. Cameron made a presentation covering his observations via the website Thinking Clinical Care, on an article called COVID Clinical Discussion.

Here you can access the audio of his lecture:

Beyond Andrew’s proposal and Dr. Camreon’s notions, a similar discussion took place covering the same phenomenon in Italy, and was published in the following white-paper: COVID-19 Does Not Lead to a “Typical” Acute Respiratory Distress Syndrome (link will open a .pdf in a new tab).

Back to Kate’s post, there are two very appealing comments that bring valid points to Andrew’s proposed theory.

The first comment is:

This might be a reach but as a physician, I’ve been aggressively treating patients here in the west with the hydroxychloroquine+high dose zinc (200mg per day)+azithromycin with good results but started getting even better when we added a true functional glutathione. We were awarded a patent on this product last year and are currently seeking several further patent continuations (along with international patents) as we were planning to create a biotech around it (meaning we already have the financing/investment and know it works like it should — first one to truly work or to be validated — the only one that works in the marketplace). And after reading these comments and this great article we believe we now know what it was doing and why — it helps prevent the cytokine cascade/storm in the lungs and the overwhelming oxidative stress as mentioned and when used along with hydroxychloroquine probably helps resolve the porphyrin problem more effectively. It is also extremely antiviral (macrophages use it to attack viruses) which is some of our first NDIs for which we are going after with the FDA. But these are all mostly just theories buttressed with the recent clinical knowledge gained by treating a lot of sick patients. Hope this helps the thoughts and conversation.

The second comment adds the following:

Now let’s move onto the haemoglobin/iron/hydroxychloroquine issue. It’s an intriguing hypothesis and would account for reports that a patient’s blood type may affect their vulnerability to the severe forms of the disease. It would also account for the fact that some patients present with symptoms of relatively mild shortness of breath (SOB — I’m not making this up; it’s a standard medical acronym) while being profoundly hypoxic (Oxygen saturation 56% (Normal = > 94%). Oddly enough, low oxygen saturation doesn’t make you short of breath. It’s the build up of CO2 that drives you to breathe even under normal circumstances. So you could be profoundly hypoxic but not short of breath as long as you could breathe out CO2. The stabilization of the haemoglobin molecule by HC (hydroxychloroquine) would be a plausible mechanism for efficacy in this situation i.e. as long as the lung damage caused by the virus/immune system cytokine storm I discussed in a previous post hadn’t taken off then the stabilization of haemoglobin and the red cell membrane would prevent the toxic effects of the free iron on the lungs (The lungs have a filtering effect because of the necessarily small capillaries they’re composed of as a consequence of having to participate in gas exchange with the outside air.) and preserve the oxygen carrying capacity of the red blood cells. Thus, HC could possibly have a doubly beneficial effect i.e. the ability to prevent the over-response of the immune system in damaging the lung and stabilize the haemoglobin molecule to prevent further lung damage by the mechanism described while preserving the oxygen carrying capacity of the red blood cell. It would be wonderful if this could be borne out!

Additionally, we have this post from Chad Roach that brings up very good points to support Andrew’s original proposal. I’ve reproduced Chad’s post here below for your convenience (or you may click here to read the original post):

Good summary, this Is a hypothesis I’ve been screaming on social media. I will add on this tidbit for you, part of my hypothesis. When the subunit is poisoned, it changes the exact shape and slope of the dissociation curve and it migrates the curve to the left. Not a typical shift left or right we think of the local factors that affect affinity. Rather the entire curve migrates to the left. The curve forthree cooperative binding sites is quite different from the curve of four. This is demonstrated in this textbook on allosteric enzyme cooperativity:

Looking at the two curves, B and C, you can imagine the hemoglobin curve somewhere in the middle. The exact shape is determined by the overall affinity. Curve a is a hyperbolic curve representing no cooperativity while the curve on the far right demonstrates cooperativity. The hill coefficient represents the degree of cooperativity and for hgb it is 2.7. When you block one of the binding sites, you block the fourth potential site which was the one with the highest afFinity and the biggest contributor to the coefficient of 2.7.

Therefore, the poisoning of the binding site migrates the entire curve to the left and dramatically increases its slope.

Remember the x-axis is Pa02.

From this migrated position you can still shift right or left depending on local factors.

But notice that the PaO2 would have to drop to very low levels before you will see a change in the amount of oxygen bound to the hemoglobin. With one site blocked, and assuming all hemoglobin is affected, the maximum O2 sat would be 75%. It’s doubtful that it’s 100% blocked and of course there is always some shunting going on, especially as the disease progresses. But the steep slope shows the lack of physiological reserve and the potential for respiratory failure, and hypoxemia in end organs, leading to failure and including arrhythmia. You are smiling and laughing on your phone with a side of 72% until you precipitously crash. Because of the steep slope.

This is why I do not recommend anyone in the hospital ambulate and the reason I think we have seen sudden death in some cases. Of course, thromboembolism is also happening and on the differential of any sudden death. I think that maximizing PaO2, avoiding exertion, minimize shunt, anticoagulation is key — until we can deactivate the virus or the viral — porphyrin moiety.

If you are as intrigued as I was, you may like to go a step further and read this: COVID-19 Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism (download pdf here). It is a highly technical document presenting several discoveries that may support Andrew’s proposed theory as well.

Before concluding, I’d like to reinforce that any content published in this News Site has its sources verified for veracity and accuracy. However, there are times – like this one now – when I feel compelled to ease my own guidelines and open space for a good discussions that offers tangible propositions behind it. Not to forget that real MD and specialists are already debating the same things, which is another good reason why Andrew’s article should deserve our attention. 

FACT: No one knows enough about the Coronavirus and the COVID-19 disease to credit or discredit any of the proposed notions about it. Notwithstanding, even if proven not to be fully accurate, Andrew’s article brings up important aspects that should be better understood while treating patients and dealing with this disease. Hence, even if it is found fundamentally wrong, it may still hold some value and help save lives in the end!

Any Comments?
Julio Marchi